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Chromosome abnormalities in 16 to 18 hour chick embryos : a study of incidence and modes of origin /Miller, Robert Christopher January 1971 (has links)
No description available.
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22 |
Chromosome abnormalities, sex ratio, and fertility in Gallus domesticus /Duber, Margaret Marie January 1973 (has links)
No description available.
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23 |
Unequal transmission of the complementary meiotic products of a gentric fission by heterozygous cocks in Gallus domesticus /Gabriel, Edward George January 1977 (has links)
No description available.
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24 |
Reproductive consequences of Z-autosome translocation heterozygosity in male domestic fowl (Gallus domesticus, L.) /Blazak, William Francis January 1979 (has links)
No description available.
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25 |
Genetic testing for susceptibility to breast and ovarian cancer : a case study of clinical decision-making in medical genetics /Glassberg, Andrea E. January 1997 (has links)
Thesis (Ph. D.)--University of Washington, 1997. / Vita. Includes bibliographical references (leaves [202]-262).
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26 |
Evaluation of consistent chromosomal abnormalities in leukemiasHood, June Lucille. January 1981 (has links)
Thesis (M. Ed.)--Kutztown State College. / Source: Masters Abstracts International, Volume: 45-06, page: 3060. Typescript. Includes bibliographical references (leaves 32-34).
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Cytogenetic and phenotypic study of long arm X isochromosome in humansFakhretaheri, Zahrabigom, 1952- January 1978 (has links)
No description available.
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28 |
Cytogenic examination of human chromosomes exposed to diagnostic ultrasound in uteroPippin, Susan Louise, 1947- January 1974 (has links)
No description available.
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29 |
A cytogenetic study of the effects of pesticides.Wuu, Kuang-Dong January 1966 (has links)
A cytogenetic study of the effects of 15 pesticides (herbicides: Alanap-3, Atrazine, Banvel D, Cytrol, Embutox E, Hyvar X, Lorox, Monuron, Simazine; insecticides: Endrin, Phosphamidon, Sevin; insect chemosterilants: ENT-50612, Metepa; fungicide: Botran) has been carried out with Hordeum vulgare and Vicia faba. [...]
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Genetic characterization of DiGeorge and related syndromes associated with 22q11.2 deletionsDemczuk, Suzanne January 1995 (has links)
DiGeorge syndrome (DGS) is a developmental defect associated with deletions in chromosomal region 22q11.2. Recently, other syndromes (Velo-Cardio-Facial syndrome, Conotruncal Anomaly Face syndrome, isolated conotruncal cardiopathy) with overlapping phenotypes have been found to be associated with deletions of a similar extent in this chromosomal region. All these syndromes have been grouped under the acronym CATCH 22 (Cardiac defect, Abnormal facies, Thymic hypoplasia, Cleft palate, Hypocalcemia, chromosome 22q11.2 deletions). In order to characterize genetically this group of syndromes, we have searched for deletions in the 22q11.2 chromosomal region by fluorescence in situ hybridization (FISH). A set of 6 cosmid probes dispersed within the whole length of the DGS deleted region was used to screen 23 patients. A 22q11.2 deletion was observed in 96% of the patients studied. Furthermore, there does not seem to exist any correlation between the size of the deletion and the phenotype observed, since the majority of patients studied, although widely divergent in their clinical manifestation of DGS, appeared to present the same extent of deletion in this genomic region. / There appears to be a predominance of deletion-bearing mothers in familial CATCH 22 when published pedigrees are examined. Furthermore, our own familial cases and the sporadic cases where the parental origin of the deletion could be deduced using a chromosome 22 short arm heteromorphisms seem to confirm this tendency. Because we had isolated a CA-repeat locus mapping within the DGS deleted region, the parental origin of the deletion in sporadic DGS/VCFS cases was studied by assessing the inheritance pattern of this microsatellite marker. The deleted portion of chromosome 22 was of maternal origin in 16 out of 22 cases (72%). When cases of sporadic, familial and unbalanced translocation inheritance reported in the literature were pooled with these results, there appears to be a net tendency for the deletions to be of maternal origin in CATCH 22 (70 deletions of maternal origin, 21 of paternal origin, X$ sp2$ = 26.4, p $<$ 0.0001). / In order to identify the molecular defect underlying DGS, we embarked on a positional cloning approach. A detailed physical map of the 22q11.2 region was made using one- and two-color FISH on metaphases and G$ sb0$ interphase nuclei, and by hybridization to a chromosome 22 hybrid panel. This permitted delineation of a critical region, within which the breakpoint of a balanced translocation carrier affected with DGS was mapping. This breakpoint was cloned by the construction of cosmid contigs, and a novel gene mapped to this region was isolated. The gene potentially encodes an adhesion receptor, and is not interrupted by the balanced translocation breakpoint. Possible mechanisms through which this gene can be involved in the pathogenesis of DGS are presented. / This research project has contributed toward the understanding of the genetics of DGS and related syndromes. Furthermore, a candidate gene for the CATCH 22 syndromes has been isolated and further work will confirm whether it plays a major role in the pathogenesis of these syndromes.
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